Heart Failure

Last updated: April 8, 2026, 4:02 PM Pacific Time (PDT)
Disease framework for heart failure across chronic phenotype and acute syndrome. Use it to recognize decompensation, separate congestion from shock, confirm the syndrome, and tailor therapy for HFrEF, HFpEF, or advanced decompensated presentations.
All Clinical risk factors Diagnostics Confirmation criteria Management Back to Main Page

Disease Pathway

risk factors -> diagnostics -> differential / confirmation -> syndrome-based management
Clinical Risk Factors

Who should trigger heart-failure reasoning?

  • Dyspnea, orthopnea, edema, weight gain, elevated JVP, pulmonary crackles, or worsening exercise tolerance
  • Known HFrEF or HFpEF, CAD, hypertension, CKD, valvular disease, atrial fibrillation, cardiomyopathy, or prior admissions for volume overload
  • Possible triggers: dietary indiscretion, medication nonadherence, AKI, arrhythmia, ischemia, infection, uncontrolled hypertension, or pulmonary embolism
  • Signs of low output or shock: cool extremities, narrow pulse pressure, hypotension, rising lactate, AKI, altered mentation
  • Think advanced or mixed physiology when congestion and hypoperfusion coexist
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Diagnostics

Order studies that fit the care setting

Core labs
  • CBC
  • CMP
  • BNP / NT-proBNP
  • Troponin
  • Lactate
Additional labs
  • TSH
  • Urinalysis
  • Blood cultures / infectious workup
Imaging / diagnostics
  • ECG
  • Chest x-ray
  • Transthoracic echo
  • POCUS
Procedures
  • Right-heart catheterization
  • Coronary angiography / ischemic evaluation
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Differential Diagnosis

Keep common mimics and parallel processes in play

Key mimics
  • Pneumonia / aspiration
  • Pulmonary embolism
  • COPD / asthma exacerbation
  • CKD with edema / volume issues
  • Cirrhosis / hypoalbuminemia
  • Primary sepsis or mixed shock without primary HF
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Confirm Diagnosis

Define both chronic phenotype and current syndrome

  • Heart failure syndrome: compatible symptoms/signs plus objective evidence of congestion, elevated filling pressures, or structural heart disease.
  • HFrEF: typically LVEF 40% or less on echo, often with LV dilation/remodeling and reduced systolic function.
  • HFpEF / preserved EF syndrome: typically LVEF 50% or more plus evidence of elevated filling pressures or diastolic dysfunction, such as left atrial enlargement, LV hypertrophy, abnormal E/e', elevated natriuretic peptides, pulmonary hypertension, or invasive hemodynamic evidence.
  • Acute decompensated HF: worsening congestion or low-output physiology requiring urgent inpatient treatment.
  • Cardiogenic shock / advanced HF: persistent hypoperfusion, hypotension, or escalating support requirement.
Phenotype mini-calculator
Use EF plus selected echo / peptide / bedside clues to suggest HFrEF, HFpEF, HFmrEF, or indeterminate phenotype.
Likely phenotype
Indeterminate
Enter EF or echo filling-pressure clues to phenotype the syndrome.
Drivers
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TTE findings
Clinical context
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Management

Organize management by the major heart-failure intervention buckets

Compare phenotype

Resident Pearls

Bedside Use

  • The two bedside questions are: is this congestion, low output, or both; and what triggered it?
  • Diuresis treats congestion, but it will not fix cardiogenic shock, severe valvular disease, or uncontrolled arrhythmia by itself.
  • BNP helps, but the diagnosis still lives in the whole clinical picture plus imaging and response to therapy.
  • Do not stop at “CHF exacerbation” without looking for the trigger: ischemia, infection, arrhythmia, PE, AKI, medication issue, or uncontrolled blood pressure.
  • Right-heart or shock physiology should prompt earlier ICU / cardiology involvement than people often think.

Sources